Suspect Pathogens

Research Studies

Alzheimers Disease: A Novel Hypothesis for the Development and the Subsequent Role of Beta Amyloid
Journal of Neuroinfectious Diseases, 2016.
“Spirochetes, biofilms, and innate immune system activity have all been recently found in the brains of Alzheimer’s disease patients. The mechanism and actions of those factors in producing the disease were discussed in those studies. However, neither the production nor the role of beta amyloid was included in the discussion of those studies. In this commentary, we hypothesize how the development of beta amyloid occurs as a result of the activation of the innate immune system first responder Toll-like receptor 2 (TLR 2) and its major pathway (MyD88). This leads not only to TNFα, but also NFκB. Both of these molecules have been previously shown to induce the secretases necessary to cleave the amyloid precursor protein. This leads directly to beta amyloid. Further, the beta amyloid (Aβ) has been shown to be antimicrobial and its presence on and around the hippocampal plaques (the pathological hallmark of Alzheimer’s disease) has been demonstrated. It becomes apparent that the Aβ tries to kill the spirochetes but cannot penetrate the biofilm. Its build-up then interrupts and destroys the brain tissue.”

Alzheimers Disease: The Novel Finding of Intracellular Biofilms
Journal of Neuroinfectious Diseases, 2017.
Abstract- “We previously have found biofilms in the hippocampi of Alzheimer’s disease (AD) post mortem brain specimens. We had seen them in an extracellular location and noted them to be present in the areas of pathological plaque formation. Other investigators have found the presence of spirochetes (Lyme and dental) in affected (AD) brains, and these have been correlated with Treponema pallidum. In a recent historical comparison of the pathology of syphilis, the histological findings of syphilis and AD were shown to be exactly the same. Further, spirochetes have been cultured from the affected brains and have been found to make biofilms and beta amyloid precursor protein. Utilizing the same pathological methods as in our prior study, we have found biofilms in an intracellular location. The similarity of this finding to other diseases has been presented; and, the impact of the “intra” versus the “extra” cellular location is discussed.”

Review Articles

Alzheimer’s Disease: A Novel Hypothesis Integrating Spirochetes, Biofilm, and the Immune System
Journal of Neuroinfectious Diseases, 2016.
Abstract- “
In the light of recent studies showing the presence of spirochetes in the brains of Alzheimer’s disease (AD) patients, we have studied (post mortem) the hippocampus region in the brains of similarly affected AD patients utilizing both pathology and immunohistochemistry. Our findings demonstrate that the plaques, which are characteristically found in AD brains, reveal the presence of biofilms. These biofilms are undoubtedly made by the spirochetes present there; further, we have also found that the biofilms co-localize with the β amyloid that is a signature finding in the disease. Also, we have shown activation of Toll-like receptor 2 in the same areas. We postulate this is related to the disease because this innate immune system molecule cannot penetrate the biofilm to destroy the spirochetes present there, so, inasmuch as it is activated, it destroys the surrounding tissue instead. We compare this destruction to that which is caused by activation of the adaptive immune system, which leads to much more severe devastation, much more rapidly.”

Alzheimer’s Disease: Assessing the Role of Spirochetes, Biofilms, the Immune System, and Amyloid-β with Regard to Potential Treatment and Prevention
Journal of Alzheimer’s Disease, 2016.
Alzheimer’s disease (AD) is an infectious disease caused by spirochetes, and these spirochetes form biofilms, which attract the innate immune system. The innate immune system first responder, Toll-like receptor 2, generates both NF-κB and TNF-α which try to kill the spirochetes in the biofilm, but cannot penetrate the “slime”. NF-κB is also responsible for the generation of amyloid-β (Aβ) which itself is anti-microbial. Aβ cannot penetrate the biofilm either, and its accumulation leads to destruction of the cerebral neurocircuitry. Treatment with penicillin (as in tertiary syphilis, the comparator to AD) is outlined; a biofilm dispersing agent may need to be added to the protocol.  Where spirochetes have been found in the brains of Alzheimer’s disease (AD), it may be considered an infectious disease; this is the first and most important consideration [1, 2]. It is also a chronic disease, a biofilm-associated disease, [3] and an autoimmune disease [4]. Further, it is a debilitating disease, a socially-destructive disease, an exceedingly expensive disease, and, lastly, a deadly disease [5]. This review will focus on the biofilm portion of the disorder as well as the autoimmune response. It will also touch on some rational therapeutic concepts for this most irrational of diseases.”

Microbes and Alzheimer’s Disease

Journal of Alzheimer’s Disease, 2016.
Abstract- “We are researchers and clinicians working on Alzheimer’s disease(AD) or related topics, and we write to express our concern that one particular aspect of the disease has been neglected, even though treatment based on it might slow or arrest AD progression. We refer to the many studies, mainly on humans, implicating specific microbes in the elderly brain, notably herpes simplex virus type1(HSV1), Chlamydia pneumoniae, and several types of spirochaete, in the etiology ofAD.  Fungal infection of AD brain[5,6]has also been described, as well as abnormal microbiota in AD patient blood [7].  The first observations of HSV1 in AD brain were reported almost three decades ago[8].  The ever-increasing number of these studies (now about 100 on HSV1 alone) warrants re-evaluation of the infection and AD concept.”

Herpes Simplex Virus Type 1 and Other Pathogens are Key Causative Factors
in Sporadic Alzheimer’s Disease
Journal of Alzheimer’s Disease, 2015
This review explores the relationship between pathogens, including Herpes simplex virus type 1 (HSV-1), Cytomegalovirus, and other Herpesviridae, Chlamydophila pneumoniae, spirochetes, Helicobacter pylori, and various periodontal pathogens and sporadic Alzheimer’s Disease.  It examines the correlation of infection with the release of pro- inflammatory cytokines that may cross the blood-brain barrier and promote neurodegeneration.

Infectious Agents and Neurodegeneration
Molecular Neurobiology, December 2012.
Abstract- “A growing body of epidemiologic and experimental data point to chronic bacterial and viral infections as possible risk factors for neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease and amyotrophic lateral sclerosis. Infections of the central nervous system, especially those characterized by a chronic progressive course, may produce multiple damage in infected and neighboring cells. The activation of inflammatory processes and host immune responses cause chronic damage resulting in alterations of neuronal function and viability, but different pathogens can also directly trigger neurotoxic pathways. Indeed, viral and microbial agents have been reported to produce molecular hallmarks of neurodegeneration, such as the production and deposit of misfolded protein aggregates, oxidative stress, deficient autophagic processes, synaptopathies and neuronal death. These effects may act in synergy with other recognized risk factors, such as aging, concomitant metabolic diseases and the host’s specific genetic signature. This review will focus on the contribution given to neurodegeneration by herpes simplex type-1, human immunodeficiency and influenza viruses, and by Chlamydia pneumoniae.”

Historic evidence to support a causal relationship between spirochetal infections and Alzheimer’s disease
Frontiers In Aging Neuroscience, 2015.
Abstract- “Following previous observations a statistically significant association between various types of spirochetes and Alzheimer’s disease (AD) fulfilled Hill’s criteria in favor of a causal relationship. If spirochetal infections can indeed cause AD, the pathological and biological hallmarks of AD should also occur in syphilitic dementia.  Historic observations and illustrations published in the first half of the 20th Century indeed confirm that the pathological hallmarks, which define AD, are also present in syphilitic dementia. Cortical spirochetal colonies are made up by innumerable tightly spiraled Treponema pallidum spirochetes, which are morphologically indistinguishable from senile plaques, using conventional light microscopy. Local brain amyloidosis also occurs in general paresis and, as in AD, corresponds to amyloid beta. These historic observations enable us to conclude that chronic spirochetal infections can cause dementia and reproduce the defining hallmarks of AD.”